When a coronary artery closes silently, cutting off the oxygen supply to an entire region of the heart, the body has only minutes to respond. Cells begin to die. Tissues starve. Yet, for reasons scientists still struggle to explain, two people with nearly identical injuries can have vastly different futures. One recovers quickly; the other carries the damage for life.

Part of the answer lies in a network of blood vessels known as collateral arteries. These vascular channels can reroute blood around a blockage, restoring oxygen to injured tissue. Some people are born with abundant collateral networks. Others have very few. Under certain conditions, however, the body can even build new ones.

My idea of an artery was embarrassingly simple: a hollow tube in an anatomy textbook, fully developed during the early years of life. Turns out, an artery knows the trick to unmake itself when it is pinched shut. Its walls loosen into individual cells that gather again and stitch together new back up vessels. Few scientists have spent as much time unravelling this mystery as Soumyashree Das.

At her laboratory at the National Centre for Biological Sciences (NCBS-TIFR), Bengaluru, Das studies how blood vessels develop, regenerate and respond to injury. Her work sits at the intersection of developmental biology and medicine, drawing together genetics, microscopy and surgical techniques to answer one simple question: How do arteries rebuild themselves?

The question is much newer than the instinct behind it.

Das grew up in Cuttack, Odisha, in a household where science was less a profession than an atmosphere. Her father taught chemistry at a university; her mother worked in finance. 

It was the little things like dinner table conversations. I remember my father bringing chemistry models home and teaching me and my sister. When you encounter science in bits and pieces every day, as part of your daily life, it inspires you — not in a cinematic way where you suddenly realise it. For me, it happened gradually. It was a series of baby steps.” 

Das told me.

Those steps did not initially lead toward biology. In school, Das considered herself stronger in physics and chemistry. But it was biology that captured her attention. She was fascinated by the body, especially by how organs functioned, how different tissues worked together and how something as intricate as a human being emerged from a collection of cells. It began as a simple curiosity, the kind that sends you flipping through diagrams of the heart or wondering what happens beneath the skin.

By the time she began her PhD at Rutgers University,New Jersey, in the laboratory of Nan Gao, those questions had turned into a fascination with cell fate. She studied how stem cells in the intestine decide whether to remain stem cells or become something else entirely. This decision is regulated in part by Wnt, a signalling pathway that plays a central role in the development and regeneration of many tissues. Das traced the stem cells’ fate to Wnt secretion and to the function of a vesicle transport protein called Rab8a, which physically carries the signal out of the cells producing it. When Rab8a is absent, Wnt secretion is disrupted, compromising the maintenance of the stem cell population. 

She didn’t move into vasculature for any grand reason. A postdoctoral position at Stanford, in the laboratory of Kristy Red-Horse, ​“just seemed like a great field to be in,” as she has put it. Red-Horse was supportive, but the question that had driven Das since her PhD—​‘what makes a cell choose one identity over another?’ remained the same. Only the biological system had changed.

The first year at Stanford nearly ended things before they began. Postdoctoral research is often demanding, but for Das, the experience felt particularly difficult. ​“Postdocs are tough because you want to do something amazing, and there is this peer pressure also because in a place like Stanford, you really need to stand out,” she said. ​“I almost quit after my first year. I was not getting anywhere, and I thought maybe academia was not for me.” 

Red-Horse talked her down. Das recalled that conversation: 

My supervisor told me, ​‘Nothing happens in a year, at least not in biology. You have to give yourself at least a couple of years to see whether you can get anywhere.’ And one thing that she said that has stayed with me, and I still tell my lab is that you have to learn to enjoy your day-to-day life. You can’t be miserable on a daily basis and hope that you are going to make an amazing discovery in the next year or ten years.” 

The part of the work that demanded Das’s attention was confocal imaging. She attached tiny fluorescent tags to cells, and every day, she watched what the naked eye never could. Arteries glowing like tree branches filled with fireflies, and coloured cells that looked like constellations. The question she was trying to answer had been lingering in the minds of biologists for years: why do some heart-attack patients survive better and recover faster than others? Red-Horse and her team suspected that the answer lay in collateral arteries. Mice were the best model because they offered one inconsistency that was useful. Newborn mice can build a working collateral artery within four to six days of an injury, but older mice mostly cannot. That gap between what a young body can do and what an ageing body can no longer do became the engine of the whole research. 

Das fluorescent labelled the coronary arteries in a set of mice. To simulate a heart attack, she tied off a coronary artery and blocked the blood flow. The surgical procedure was led by cardiothoracic surgeon Andrew Goldstone, who was then a medical resident at Stanford. She returned every six, twelve, and twenty-four hours to image what the labelled tissue was doing. Individual cells broke loose from the walls of the injured artery and migrated outward into the surrounding tissue. There they began to divide and then organised themselves into a new functional vessel — a bridge connecting the wounded artery to a neighbouring healthy artery. The process came to be known as Artery Reassembly.

Collateral arteries are not a new discovery. As early as the 2^nd century AD, the Greek physician Antyllus had noticed that major blood vessels in the limbs could be tied off without killing the tissue beyond them. Das traces the next chapter of the story to the 17^th century, when the English physician and anatomist Richard Lower injected dye into the coronary arteries of a human heart after death and watched it flow into the territory of another vessel. Centuries later, studies showed that patients with collateral arteries recover better from strokes and heart attacks than those without them. But were these hidden detours already there as emergency lifeboats, or could the body build new ones after blood flow was cut off? Das’s postdoctoral research went further than almost anyone before her in answering that question. It didn’t just show that collateral arteries could form after a blockage. It captured, cell by cell, the moment an artery began forming a collateral artery after a heart attack. 

Das joined NCBS, Bengaluru, as an assistant professor in 2020, stepping into the unfamiliar role of principal investigator. Her lab now runs two parallel investigations into collateral formation, one in the heart and the other in the brain. In the heart, as her postdoctoral work showed, collaterals appear during development and in response to artery blockage. In the brain, her lab has found that the tips of two separate arteries simply grow toward each other and form collaterals during normal embryonic development. A trail of cells coming from blood capillaries seems to guide the two artery tips to one another. One receptor, VegfR2, seems to matter in both organs. Another receptor called Cxcr4 is essential only for the heart’s version of the process.  In 2024, Das’ work won the Werner Risau Early Career Investigator Award in Vascular Biology, named for one of the field’s founding figures. The award recognised her discovery that arterial cells, long thought to be terminally differentiated, can re-enter the cell cycle and de-differentiate, reverting to a more potent cellular state.

Das’s working hypothesis has to do with how differently those organs tolerate a shortage of oxygen. Neurons have far less patience for it than heart muscles, which may be the reason the brain forms its emergency detours in advance rather than waiting until injury strikes. The number of collateral arteries in the brain isn’t fixed for life. It declines with age. This could be why older people are more vulnerable to strokes. 

Here is where the Wnt signalling pathway makes an unexpected reappearance. Her lab had already identified a specific Wnt ligand, WNT2, as a key regulator of collateral artery growth in the heart. The obvious next question was whether variations in this same pathway might explain why some patients recover much more poorly than others after a heart attack. In collaboration with Perundurai Subramaniam Dhandapany, faculty at Institute for Stem Cell Science and Regenerative Medicine (BRIC-inStem), Das’s lab compared the exomes (the protein-coding parts of the genome) of Indian patients with cardiovascular disease with those of healthy controls, focusing specifically on genes within the WNT signalling pathway. They found multiple genetic mutations with the potential to influence collateral artery development. The lab is now working to understand how each of these mutations affects cellular function and vascular regeneration. 

Das is already thinking beyond the laboratory and towards what these discoveries could mean for patients, long before a heart attack occurs. ​“If you know at an early stage that you have this critical mutation,” she says, ​“you will be careful about your diet and other lifestyle choices.” Her next goal, and perhaps her most ambitious, is to develop a predictive mathematical model that could use a person’s genetic profile and estimate, in advance, the kind of collateral response their body can build or support.

None of the achievements in Das’s laboratory happened under ideal conditions. Das joined NCBS in the middle of India’s second wave of COVID-19, tasked with establishing a wet laboratory thousands of kilometres away from the mentor and mouse colony she’d spent years building at Stanford. She shipped her mouse lines to Bengaluru, then spent two anxious weeks tracking a shipment that repeatedly stalled in transit, ensuring the animals were fed and watered at every delay. Almost as disorienting, in its own way, was the bureaucracy. As a graduate student and postdoc abroad, she had been shielded from the administrative side of running a lab by her own supervisors and their dedicated staff. Back in India, she found herself planning months in advance just to order a single reagent, routed through layers of approval that, she says, would have taken days rather than months anywhere else she had worked. When she started her own lab, she had imagined remaining a hands-on experimental biologist, doing experiments herself, teaching the delicate ligation surgeries personally, sitting down to analyse her own imaging data. Instead, she discovered that leading a laboratory required an entirely different set of responsibilities. Between writing grants, recruiting students and research scholars, and managing administrative paperwork, the job of a principal investigator turned out to be something very different from the one she had anticipated.

Das hopes some of that support will come through the EMBO Global Investigator Network, which she joined only recently and is still learning to navigate. The network’s training sessions have already caught her attention. Next year, more than six years after starting her own lab, she will attend her first workshop on leadership and student recruitment.

For Das, curiosity should always lead science. Where the system falls short, in her view, is not in the students, but in the support structures surrounding research. ​“Our students are as good as any other place. I have seen this first-hand after working in two different countries and having friends who have worked across the globe,”says Das. Postdoctoral researchers are often told, almost as an article of faith, that a stretch abroad is absolutely required before returning to India to lead a laboratory, advice she has heard repeatedly without anyone clearly articulating why. As a PI, she argues that funding is only part of the challenge. Scientists need institutional support just as urgently — people who can handle travel requests, purchase orders, and the administrative work that quietly accumulates around research. While institutions like NCBS have some of these support systems in place, Das points out that access to such support remains uneven across the country. In many of the laboratories where she trained abroad, those tasks belonged to dedicated administrative staff, who supported either one PI or a small group of two or three PIs. In India, they tend to find their way back to the scientist’s desk.

NCBS has the freedom to pursue the questions that interest me and the opportunity to work with extraordinary students. Being part of this research community in Bengaluru also makes collaborations easier, with researchers often finding opportunities to work together across disciplines,” 

says Das, reflecting on her time at the institute.

Das arrived at the heart by chance. Years earlier, she had set out to understand a fundamental question in biology: how cells decide what they will become. Somewhere along the way, that question led her to collateral arteries, and to a phenomenon that seemed to defy the tidy diagrams of an anatomy textbook. A cell that has spent years as part of an artery can become something else entirely as a last attempt to bargain with death. There is something reassuring about that. That even in an organ starved of blood, some cells find new roads to life.